Sunday, September 10, 2017

Topic Discussion: Baclofen and ESRD

Baclofen is often used as a muscle relaxant in many patients. It has a half life of 3-7 hours and 80% excreted by the kidneys.  It is extremely important to dose adjust in CKD and avoid use in ESRD patients. Dialysis is a good mechanism to remove the agent as well in-case of ingestions and overdoses.

A recent case published in AJKD highlights this important drug related interaction in CKD and ESRD patients. 
The authors describe two excellent clinical algorithms.
The first algorithm discusses dose adjustments.
If GFR>90, no dose adjustment necessary
If GFR 60-90, decrease initial dose by 1/3
If GFR 30-60, decrease dose by ½ and watch for mental status changes
If on RRT or GFR<30, avoid use


The second algorithm discusses if there is a known baclofen toxicity( seizures, hypotenia, encephalopathy, etc.)

If severe AKI, CKD or ESRD- start daily HD or CRRT
If normal renal function or mild AKI but with respiratory depression or seizures- start daily HD or CRRT
If normal renal function or mild AKI and no severe symptoms- no dialysis

Tuesday, August 29, 2017

Consult Rounds: Tamoxifen induced hypercalcemia

A forgotten cause of hypercalcemia we need to remember is the drug- tamoxifen

This chemotherapy agent used in breast cancer has had a track record of causing hypercalcemia.
It was first described in 1980s.  In that large study, 470 patients with metastatic breast cancer treated with tamoxifen, ten patients (2.3%) developed hypercalcemia. All patients with hypercalcemia had osteolytic or mixed lytic and blastic bone metastases. Hypercalcemia developed after a median period of seven days (range 4-11 days) of tamoxifen administration. Hypercalcemia was treated with conventional measures and serum calcium levels normalized in nine patients, either with a brief interruption of tamoxifen therapy or in spite of continued treatment. Four patients experienced partial remissions with continued tamoxifen therapy. These results indicate that hypercalcemia is a potentially serious complication of tamoxifen therapy but is generally short-lived, and can be controlled with supportive measures, thus allowing continued tamoxifen administration.

Other published reports are

One recent study looked at a large series of breast cancer patients who were hypercalcemic post tamoxifen- happened within 9 days of start and peaked at a level of 13. All patients also had bone lesions as well.  Gallium nitrate was used to reverse the abnormality while keeping tamoxifen on.


No mention of this in any renal literature. Unclear mechanism of this entity. 

Monday, August 28, 2017

Topic discussion: Downsizing in Nephrology

A timely editorial just got published in CJASN. 
Three large NYC related programs give their thoughts on downsizing in nephrology fellowship spots. A comparison is made with anesthesiology that helped revert their trend of decrease supply in the 1990s.  The authors bring up few major concerns

1.       The debt burden of recent graduates and the compensation that nephrologists receive is not attractive. But the authors make a good point that while the starting salaries are low, there is room for growth and potential that other fields might not have. This is speculative and might depend on coast to coast in the US. While certain parts of the country, nephrologist make a lucrative salary, there are others where hospitalists make much more than nephrologists.

2.       The authors make an interesting suggestion of broadening our certification. This is an excellent thought. I urge the nephrology community to try to do this in the 2-3 year time frame of a fellowship. There are a minority of candidates who would do an extra year given their debt burden but incorporating something extra in your fellowship might help that candidate get that certificate along with Nephrology- be it glomerular disease, onconephrology or critical care.

3.       Chronic disease models have done well with PA and NP based teams in certain parts of the country. Examples are oncology, BMT, renal transplant, CT surgery. Nephrology should learn from these models. As the authors suggest, perhaps cautious downsizing might help reverse trend of supply/demand and help get outstanding candidates back in Nephrology.  A formula was suggested back few years ago by Desai and perhaps can be considered if need be.

4.       Overnight call is part of being a nephrologist. While authors suggest that the fellows might be called in a lot- one cannot ignore a K of 8 and wait till the 8AM fellow/attending comes in. Remote management might be possible but we have to be cautious in those methods.  Transplant overnight call should be reduced and can be the most helpful. A DDRT call should really not involve the nephrology fellow unless dialysis is required pre transplant. 

5.       Regardless of number of applicants a program is getting- the dependence on fellows for day to day work should be abolished.  This makes the applicant feel that the program is “fellow” centric and not “fellow” dependent. Attending directed services, NP, and PA based practice can help foster this environment. The flip side is loss of intensive education.  Given the rounding in the dialysis unit to only an NP or PA and relieving the fellow might lead to long term loss of education that we may regret. If planning this, would careful involve fellow in some of the rounding as well.  In addition, taking care of certain volume of patients and putting a cap on consults can also lead to “inefficient” graduates and unable to handle the volume when in private practice.  Fellows also have to learn how to manage and prioritize sick vs not that sick patients and how to manage a long and busy list. Nephrologists are smart physicians. We also want our fellows to be effective communicators, and efficient doctors.



I commend the authors on this very provocative essay and hoping this dialogue continues in making nephrology more attractive as it was many years ago.  

Wednesday, August 9, 2017

Monday, August 7, 2017

Saturday, August 5, 2017

Friday, August 4, 2017

Consult Rounds: Parvovirus b19 and Glomerular disease


Image result for parvovirus b19Parvovirus b19 has been associated with the following glomerular findings


1.  Collapsing GN
2. Proliferative GN
3. FSGS
4. Thrombotic Microangiopathy

https://www.ncbi.nlm.nih.gov/pubmed/17699510 in an amazing review article that summarizes all renal associated findings with parvovirus b19 especially in the transplanted kidney.

Friday, July 14, 2017

Topic Discussion: CAR-T therapy and the Kidney



A new dawn is breaking in the field of hematologic malignancies, as the first product based on chimeric antigen receptor (CAR) T cells was scrutinized today by a panel of experts and unanimously recommended for approval at the FDA for pediatric and young adult patients (age 3-25 years) with relapsed or refractory acute lymphoblastic leukemia (ALL).


Blood is collected from the patient, and then autologous T cells are separated out and genetically engineered. The process involves inserting a CAR that targets CD19, an antigen expressed on B cells and tumors derived from B cells.  These CAR T cells are then infused back into the patient, who has undergone chemotherapy, and in the body the product homes in on B-cell leukemic cells and destroys them.  The main action happens mostly about 2 weeks after those CAR-T cells have been re-infused.  Some have termed this form of therapy as the “ living drug”

Autologous CAR-T cell therapy first shot into headlines about 4-5 years ago when it was thought about in CLL patients.   Then several other studies were done essentially confirming that the concept is correct but there are serious toxicities.


The technology is complicated and initially when tried in CLL led to multiple toxicities of various organs including CNS, cardiac, renal and mostly requiring ICU admissions from acute cytokine release syndrome. This happens due to high levels of IL-6, a cytokine that is secreted by T cells and macrophages in response to inflammation.  Etanercept and tocilizumab have been used to block the IL-6 activity to treat such side effects.

Acute renal injury following CAR T-cell infusion is multifactorial and almost always reversible. Reduced renal perfusion is often the most important cause of renal injury. Reduced renal perfusion can be caused by cytokine-mediated vasodilation, decreased cardiac output, or intravascular dehydration due to insensible losses from high fevers. Tumor lysis syndrome and drug effect from medications such as antibiotics are other possible causes of renal injury. Electrolyte disturbances, such as hyponatremia, hypokalemia, and hypophosphatemia are not uncommon but have been reported. A recent article in Blood summarizes all toxicities.

Now the therapy has returned and we may see this in many centers. We must be aware of the cytokine release storm that it can cause leading to AKI in that setting.  There might be more in the pipeline of similar products such as the one that just got approved for ALL.




Consult Rounds: Cholemic nephrosis or Bile cast nephrpathy or should we say Jaundice associated nephropathy













Bile cast nephropathy or also called cholemic nephrosis represents a spectrum of renal injury from proximal tubulopathy to intrarenal bile cast formation found in patients with severe liver dysfunction. Bile can be toxic directly to the tubule or can form casts and have similar damage as myeloma cast nephropathy.


1.      Classically seen with patients with acute or chronic liver disease
2.      Usually, the total bilirubins are over 20 and conjugated over 16 is the cases that had bilirubin casts on kidney biopsies
3.      The LFTS were also higher in these patients
4.      The cause of liver disease doesn’t matter

The mechanisms responsible for tubular dysfunction include uncoupling of mitochondrial phosphorylation (thereby decreasing ATPase activity) by bilirubin  and oxidative damage of tubular cell membranes as well as inhibition of Na-H and Na-K pumps in the tubular cell membranes by bile acids. Cholemic nephrosis is reversible provided bilirubin levels are reduced early. This recovery is however delayed if there is extensive bile cast formation.
Some have suggested jaundice-related nephropathy as a replacement for cholemic nephrosis. Based on their definition, jaundice-related nephropathy would encompass the spectrum of injury that ranges from proximal tubulopathy to extensive tubular injury and tubular pigment. 
As bile passes via tubules, there is pigment nephropathy.

Pathology findings include: extensive acute tubular injury with bile stained tubular casts.
Macroscopic findings will include bile stained yellowish discoloration of the kidneys in jaundiced patients which become dark green after formalin fixation.
The Hall's stain confirms bilirubin presence.

Other interesting articles on this topic

Saturday, July 1, 2017

Consult Rounds: Acyclovir and dialysis



An often unforgotten drug that we must be aware of in ESRD patients is acyclovir.
Acyclovir can accumulate in ESRD if not dosed appropriately and can lead to neurotoxicities- leading to confusion, tremors and coma.

Initial study of 7 patients with end stage kidney disease receiving hemodialysis looked at levels following hemodialysis with each patient received a single 800-mg tablet of acyclovir. Plasma acyclovir levels were monitored over the next 48 h as well as before and after the next routine dialysis. Peak plasma levels were achieved at 3 h (12.54 +/- 1.76 microM, range 8.5-17.5 microM) with the half-life calculated to be 20.2 +/- 4.6 h. Mean plasma level of 6.29 +/- 0.94 microM were within the quoted range to inhibit herpes zoster virus (4-8 microM) at 18 h. Hemodialysis (4-5 h) eliminated 51 +/- 11.5% of the acyclovir which remained at 48 h. Computer modelling of various dose modifications suggests that a loading dose of 400 mg and a maintenance dose of 200 mg twice daily is sufficient to maintain a mean plasma acyclovir level of 6.4 +/- 0.8 microM. A further loading dose (400 mg) after dialysis would raise the residual acyclovir concentration by 6.1 +/- 1.0 microM.

Acute acyclovir neurotoxicity can be treated in CKD and ESRD patients with dialysis. The drug is water soluble, not albumin bound and small- hence an ideal dialysis candidate for removal.  It is important to keep this toxicity in mind as many might come in to your office with non renal dosing of this agent on ESRD and CKD patients and can lead to neurotoxicity. PD is not an option; HD is preferred mode for removal of acyclovir. 

  Some references

Tuesday, June 27, 2017

Topic Discussion: New Glomerular diseases cases with targeted therapies

Targeted therapies can lead to a glomerular disease. Previously, two reviews didn’t find any glomerular diseases associated with BRAF inhibitors and PD-1 inhibitors.  In the last 6 months, 3 recent papers have highlighted interesting cases of both BRAF-MEK combination and PD-1 inhibitors leading to glomerular diseases.

  

While the PD-1 inhibitor case is the first of it’s kind, we must be mindful of GN in these patients as well. In terms of the BRAF+MEK combo, both authors of the above listed papers. Showed that it was the BRAF inhibition that decreased PLCε1 expression in podocytes, accompanied by a reduction in nephrin expression and an increase in permeability to albumin. Additionally, these drugs inhibited the podocyte–vascular endothelial growth factor (VEGF) system leading to perhaps a component of TMA as well.


Tuesday, May 30, 2017

ASN Robert G Narins Award for 2017 goes to Blogger, educator Joel Topf

The Robert G. Narins Award by ASN honors individuals who have made substantial and meritorious contributions in education and teaching. This award is named for Robert G. Narins, who is also the first recipient of the award.

Dr. Narins' contributions to education and teaching started in 1967 from chairing for eight years the ABIM's Nephrology Board and working on the ACP's Annual Program Committee. His contributions to education in the fields of fluid-electrolyte and acid-base physiology are prodigious and well-recognized.  Dr. Narins was also involved in the creation and planning of many ASN educational programs during Renal Week and throughout the year, including: Board Review Course and Update, one and two day programs at Renal Week, Renal WeekEnds, and NephSAP.

Prior Award winners of this award are( from ASN website)

·    2015 Mark L. Zeidel, MD, FASN
·    2014 Stuart L. Linas, MD, FASN
·    2013 Mark E. Rosenberg, MD, FASN
·    2012 Donald E. Kohan, MD, PhD, FASN
·    2011 Agnes B. Fogo, MD
·    2010 Barry M. Brenner, MD
·    2009 Burton D. Rose, MD
·    2008 Mitchell L. Halperin, MD
·    2007 Richard J. Glassock, MD
·    2006 Robert G. Narins, MD

This year marks a landmark in this award as it’s being presented to Joel Topf, MD.

Image result for joel topf

While all other educators followed a conventional track for teaching and educating, Joel’s contribution to nephrology education has been very unique and different.  Here is what Joel has accomplished in the last 10 years!
1.       Creation and maintaining the Precious Body Fluids Blog with educational material that spans from electrolyte disorders to AKI
2.       The best acid base book written in Nephrology as a “resident”. This is by far the easiest book to understand acid base disorders.
3.       Co creation of the first ever academic journal blog- AJKD blog
4.       Creation of Nephmadness since 2013 ( first ever online game in Nephrology) with educational material that spans all parts of renal medicine
5.       Creation of NephJC( the first and most successful online journal club that meets every 2 weeks)
6.       Co creation of DreamRCT( how to propose and create a dream RCT that we need in nephrology competiton)
7.       Creation of Nephrology Social Media Collective Internship to train trainees, and faculty on become social media experts to improve medical education
8.       Teaching and promoting social media education in nephrology
9.       Showcasing how twitter can be used in nephrology education at it’s best! (https://twitter.com/kidney_boy)
10.   Several teaching awards at his local institution

Most important of all: He has inspired and trained many young and old teachers/and educators due to his passion for nephrology!
Way to go Joel and congrats!

Wednesday, May 17, 2017

Consult Rounds: Topiramate and the Kidney

Topiramate was first introduced to treat seizures but now is increasingly used to treat migraines and is among the top 6 drugs sold in the United States. In addition, it is used as a weight loss agent as well. Renal toxicity with this agent is not uncommon.

The three forms of renal toxicity are:

Kidney Stones
Renal Tubular Acidosis
Isolated hypokalemia

A study in 2006 published in AJKD showed that topiramate acts through multiple mechanisms, 1 of which is the inhibition of carbonic anhydrase, as in vitro studies have shown. Several case reports described a link between topiramate and the formation of calcium phosphate stones, but the mechanism for this is largely unknown.

The authors conclude that taking topiramate for about 1 year caused systemic metabolic acidosis, significantly increased urine pH, and markedly lowered urine citrate — changes that increase the propensity to form calcium phosphate stones.

With the increasing use of topiramate, reports have emerged that topiramate can cause metabolic acidosis in some patients. It does this by impairing both the normal reabsorption of filtered HCO(3)(-) by the proximal renal tubule and the excretion of H(+) by the distal renal tubule. This combination of defects is termed mixed proximal and distal RTA. Topiramate-induced RTA can make patients prone to kidney stones as stated earlier as well.  The utility of regular monitoring of HCO(3)(-) levels has not been proven and is not routine practice currently.

Finally, isolated refractory renal wasting of potassium has also been reported with this agent.

A large systematic review confirmed the above findings of renal toxicity with this agent. Fourty-seven reports published between 1996 and 2013 were retained for the final analysis. Five case-control studies and six longitudinal studies addressed the effect of topiramate on acid-base and potassium balance. A significant tendency towards mild-to-moderate hyperchloraemic metabolic acidosis (with bicarbonate ≤21.0 mmol l(-1) in approximately every third case) and mild hypokalaemia (with potassium ≤3.5 mmol l(-1) in 10% of the cases) was noted on treatment with topiramate, which was similar in children and adults.

Finally,increasing evidence supports the use of topiramate. Topiramate is generally well tolerated, and serious adverse events are rare. Nonetheless, it is linked with the development of acidosis, hypokalaemia, hyperuricaemia and hypocitraturia and eventually renal stones.



Monday, May 15, 2017

Master teacher: how do you define one?

Image result for master teacher

What makes a “master clinician teacher”—adapted from George Couros, an educator.

This list can be used for teachers in med students, residency and in nephrology fellowship as well.

·         Connects with students and gets to know them individually.
·         Helps students to meet their own individual needs as each might have their own learning styles
·         Makes the curriculum and what is taught relevant.
·         Works with students to develop their love of learning, helping students to find their own spark in learning( concept of intrinsic motivation –often lacking in our trainees)
·         Keeps themselves as a teacher up-to-date. Education and learning will always change ( being a learner for life makes you a better teacher)
·         Focuses on learning goals as opposed to performance goals.
·         Ensures that “character education” is an essential part of learning. Students need to grow emotionally as well as mentally( this is critical in creating the culture for constant life long learning and work life balance)
·         Is passionate about the content they teach( THIS is by far the MOST important quality)
·         Is concerned not just with what is taught in their class but with their overall impact on the school culture( Making a cultural difference is critical on perhaps methods of teaching)
·         Communicates well with all the stakeholders and not just the students( a subtle but needed politician)

·         Behaves as a facilitator of learning- not a “spoon feeder”


All our fellows out there, I am sure you have one mentor who exemplifies these qualities. This is what makes the experience of learning a more meaningful experience. Please take a minute to salute and respect all our teachers and educators in our lives. They teach you medicine but they also may be teaching you a way of life!

Tuesday, May 9, 2017

In the NEWS: Too much salt intake doesn't lead to increased water drinking

Two published studies in JCI might change how we think the body handles “too much salt”


What we learnt in medical school:

If you eat a lot of salt — sodium chloride — you will become thirsty and drink water, diluting your blood enough to maintain the proper concentration of sodium. Ultimately you will excrete much of the excess salt and water in urine.

When salt intake was increased in Russian cosmonauts studied, the urine Na excretion did increase as expected. But, the urine volume was not associated with those changes. When salt intake was high, the folks drank less water in the long run and still excreted increased water amounts. Where was this extra water coming from? The crew members were increasing production of glucocorticoid hormones, which influence both metabolism and immune function and allowed fat breakdown leading to water production.

Taking these observations to the lab, the investigators began a study of mice in the laboratory. The more salt the investigators added to the animals’ diet, the less water the mice drank(counter to what we think science teaches us when we eat a high salt diet). The animals were getting water by not drinking it but via  increased levels of glucocorticoid hormones breaking  down fat and muscle in their own bodies. This freed up water for the body to use.
Now published, the authors report the unexpected observation that long-term high salt intake did not increase water consumption in humans but instead increased water retention. Moreover, salt and water balance was influenced by glucocorticoid and mineralocorticoid fluctuations. 
This leads to a even bigger question? – does high salt intake= potential weight loss as fat breakdown is happening? So in other words, a high salt intake body is behaving similar to a starving body.

 I am sure that there is more to it!  In the long run, this is probably not a good adaption of the body and high glucocorticoid state is likely a risk of diabetes.  But these studies show us that we really don’t understand salt homeostasis in humans as we thought we did.

Bravo to the scientists on publishing this alternate view on salt intake and water production.

Monday, May 1, 2017

In the NEWS: AKI and marathon runners

An interesting study in AJKD published revealed a possible risk of AKI with marathon runners. This is the first study to evaluate urine microscopy in parallel with conventional and novel biomarkers of injury and repair in marathon runners. The authors prospectively showed that the AKI in runners is secondary to structural injury, mainly acute tubular injury, as evidenced by serum creatinine levels, urine microscopy analysis, and levels of novel biomarkers of injury and repair.

One would expect these changes likely were related to elevated CPK levels and rhabdomyolysis.  Interesting, while the subjects had high CPK levels, they did not correlate with AKI episodes. The authors hypothesize that heat stress and increase in core body temperature along with systemic inflammation are likely associated with AKI in marathon runners. They said that this might be similar to the CKD that is prevalent in Central American in sugarcane workers. Agricultural workers have been shown to have acute decreases in kidney function and progression to CKD associated with dehydration, systemic inflammation, and oxidative stress.  It is also possible that compared with agricultural workers, marathon runners have controlled ischemic preconditioning throughout their training, which may improve the kidney’s ability to better tolerate repeated injury.  That is an interesting analogy.


82% developed AKIN defined stage 1 and 2 AKI. A total of 16 (73%) runners were scored as having positive microscopy findings on day 1 or day 2. Some ( minor amount ) were taking NSAIDS but 50% were on some form of herbal medications.  Regardless, this is an interesting study and perhaps should be repeated in a larger marathon population such as the NYC marathon. In addition, curious what the hyponatremia incidence was? 

Monday, April 10, 2017

Topic Discussion: Capillary Leak Syndrome

A recent review in KI summarizes the pathophysiology of capillary leak syndrome and numerous etiologies that can cause it along with an interesting management strategy.

Besides sepsis, capillary leak syndrome(CLS) can be seen in:

1.       Drug induced CLS—classically interleukin 2, gemcitabine and certain monoclonal antibodies such as OKT3, anti CD-28 antibody TGN1412  ( steroids can help treat)
2.       Engraftment syndrome- seen post HSCT ( usually 4-7 days post) with increased inflammatory markers and AKI( 12-25% in most HSCT patients)( steroids can help treat)
3.       Differentiation syndrome( retinoic acid) – steroids help in this situation as well
4.       Ovarian hyperstimulation syndrome(OHSS)—two variants( early time course, vs late following HCG treatment)—supportive care
5.       Hemophagocytic lymphohistiocytosis
6.       Hemorrhagic fever( viruses such as Ebola, Marburg, Puumala)
7.       Clarkson’s disease( idiopathic CLS)—supportive therapy, IVIG, theophylline
8.       Others:- snake bites, Ricin overdose, APLAS, Kawasaki disease

In addition to hypotension, cytokines are likely to be important in the pathophysiology of acute kidney injury in capillary leak syndrome. Fluid management is a critical part of the treatment of capillary leak syndrome; hypovolemia and hypotension can cause organ injury, whereas capillary leakage of administered fluid can worsen organ edema leading to progressive organ injury.
The first phase of treatment is volume resuscitation including fluids, pressors and or IV albumin. The second phase includes loop diuretics, diuretics with albumin and finally renal replacement therapy.

Full article here

Sunday, April 9, 2017

Case 90: Answers and Summary

Which of the following is a risk factor for bleeding post kidney biopsy?


This is a tough question. Traditionally, many have thought that ASA is a known risk factor for bleeding post kidney biopsy. A recent large study states otherwise. In a large observational study published in CKJ, >2000 patients were reviewed. The incidence of major bleeding was 2.2%.  The risk factors as assessed by statistics were need for emergent biopsy as oppose to elective renal biopsy. No major risk was noted with ASA use and BMI.  There is data from prior studies suggesting no major risk with amyloidosis unless there is a factor XII deficiency associated with the amyloidosis. Emergent need for a kidney biopsy seems to be the major risk factor more than the others. 


Tuesday, March 21, 2017

Consult Rounds: Pathology of Pre-eclampsia

Image source: JASN 2007

What do you find in the kidney biopsy of a patient with pre-eclampsia?
The immunofluorescence findings are somewhat variable with fibrin deposition often being a prominent feature.



The renal biopsy findings of preeclampsia closest to look in the context of the pathologic patterns seen in thrombotic microangiopathies (TMA). The lesions of preeclampsia share some similarities with and also some differences from those of non-preeclamptic TMA, likely owing to their differing pathogenesis.

What is the LM finding?

The glomeruli are enlarged and solidified (“bloodless”), as a result of narrowed or occluded capillary lumens that are the result of swelling of the native endothelial cells and, to a lesser extent, mesangial cells. The endothelial changes are limited to the glomerular capillaries; arterioles are typically unaffected. Thrombosis by light microscopy is decidedly unusual. In marked contrast, in nonpreeclamptic TMA, thrombosis of vessels and/or glomeruli is a central finding. Cases of severe preeclampsia with accompanying vascular thrombosis often have clinical signs suggesting a superimposed nonpreeclamptic TMA. In severe cases of preeclampsia, in particular as the lesions evolve/resolve, mesangial interposition can be seen, a finding shared with other entities resulting from chronic endothelial insult, such as “chronic” TMA or transplant glomerulopathy. So essentially, it may appear on LM in some cases- as an MPGN pattern of injury ( without the IF being positive for complements or immunoglobuins). This form of injury is termed “Glomerular endotheliosis” 

What is the EM finding?

Ultrastructural analysis will show endothelial cells with loss of fenestrations with cytoplasmic swelling, owing to fluid and lipid accumulation and capillary occlusion.

What is the IF finding?


How is it different from your “classic” non preeclamptic TMA that you might see with SLE or APLAS or in TTP?

The main finding in the “classic” TMA is thrombosis of vessels and glomeruli as the main finding with some endotheliosis. This is a rare finding in pre-eclampsia related TMA unless it is very severe.


Here is a link to a nice review:

Saturday, March 11, 2017

#Visual Abstracts: History and Future in Medicine and Nephrology

Visual abstracts have flooded the social media world in the last few months. Where did this come from and how does it impact nephrology sharing of knowledge?

Looking back I found that these existed for many years in Chemistry journals –also called graphical abstracts.  Visual or graphical abstracts are visual elements that are clearly and in short figure formed conveying the main message of the research( or review) paper.  They are self explanatory and together with the title of the paper convey the main message of the article. Given the current attention spans of readers being short and many learners being “visual”, this method can be quite effective. Journals in medicine are trying to play with this concept for their specific fields.

Dr. Andrew Ibrahim(https://www.surgeryredesign.com/) , creative director of Annals of Surgery began this revolution in Medicine. As per a twitter chat, he mentioned “ We pitched this idea to the editors of Annals of Surgery and they loved it. It was clear in June 2016 that it disseminated faster. This led to a case control cross over of 44 articles between July and Dec 2016 and results are preliminary results are promising.  The articles got read three times more if they had a visual abstract!! Once in Dec 2016, I shared my primer, there are around 20 other journals doing this.”






In the world of Nephrology, Joel Topf took on this venture for Nephjc.com and visual abstracts appeared for the first time in renal world at recent journals club in Fall of 2016.






Following that, the #nephmadness 2017 has featured many visual abstracts, some pasted below




To top it all, CJASN is the first renal journal to enter in the visual abstract world. Great start and totally amazing to have a renal journal embrace this!


Here is an image showing early leaders of visual abstracts ( courtesy Andrew)



Few that I have done




How to create them? Check  out this primer by Andrew
You can create both static and animated abstracts- both can be very important in relaying your message.  I would urge all educators to try this out.

This could make fellowship journal club more fascinating. Make your residents/fellows create them. All researchers should simplify their ideas using such techniques.  All medicine journals should strongly consider this modality.

A new wave of presenting research has arrived- #visual abstracts!

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